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Submitted on December 19, 2005
Accepted on April 21, 2006
Faculty of Medicine - Endocrinology, Memorial University of Newfoundland, St. John’s, Newfoundland, A1B 3V6, Canada; University of Texas MD Anderson Cancer Research Center, Houston, TX 77030
* To whom correspondence should be addressed. E-mail: ckovacs{at}mun.ca.
The maternal skeleton rapidly demineralizes during lactation to provide calcium to milk, responding to the stimuli of estrogen deficiency and mammary-secreted parathyroid hormone-related protein (PTHrP). We used calcitonin/calcitonin gene-related peptide-
(Ctcgrp) null mice to determine whether calcitonin also modulates lactational mineral metabolism.
During 21 days of lactation, spine bone mineral content (BMC) dropped 53.6% in Ctcgrp nulls vs. 23.6% in WT siblings (P < 0.0002). After weaning, BMC returned fully to baseline in 18.1 days in Ctcgrp nulls vs. 13.1 days in WT (P < 0.01). Daily treatment with salmon calcitonin from the onset of lactation normalized the losses in Ctcgrp nulls while CGRP or vehicle was without effect. Compared with WT, Ctcgrp null mice had increased circulating levels of parathyroid hormone and up-regulation of mammary gland PTHrP mRNA. In addition, lactation caused the Ctcgrp null skeleton to undergo more trabecular thinning and increased trabecular separation compared with WT.
Our studies confirm that an important physiological role of calcitonin is to protect the maternal skeleton against excessive resorption and attendant fragility during lactation, and reveal that the postweaning skeleton has the remarkable ability to rapidly recover even from losses of over 50% of skeletal mineral content.
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